Gut microbiome and liver diseases

Tilg, Herbert; Cani, Patrice D.; Mayer, Emeran A.

doi:10.1136/gutjnl-2016-312729

Cited by 412 publications

(269 citation statements)

References 96 publications

(81 reference statements)

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“…The normal gut microbiota carries out specific functions in host nutrient metabolism, xenobiotic and drug metabolism, structural integrity maintenance of the gut mucosal barrier, immunomodulation, and protection against pathogens 11, 12, 13, 14, 15. Recently, the gut microbiome has been shown to play a crucial role in health, as well as in diseases such as obesity,16 inflammatory bowel disease,17, 18 diabetes,19, 20 non‐alcoholic fatty liver disease,21, 22, 23 and several types of cancers 24, 25. Experimental evidence indicates that the human intestinal microbiome can influence tumor development and progression in the gastrointestinal tract by damaging DNA, activating oncogenic signaling pathways, producing tumor‐promoting metabolites, and suppressing the antitumor immune response 7, 25, 26, 27, 28, 29.…”

Section: Introductionmentioning

confidence: 99%

Review of the gut microbiome and esophageal cancer: Pathogenesis and potential clinical implications

Baba

Iwatsuki

Yoshida

et al. 2017

Annals of Gastroent Surgery

101

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Esophageal cancer ranks among the most aggressive malignant diseases. The limited improvements in treatment outcomes provided by conventional therapies have prompted us to seek innovative strategies for treating this cancer. More than 100 trillion microorganisms inhabit the human intestinal tract and play a crucial role in health and disease conditions, including cancer. The human intestinal microbiome is thought to influence tumor development and progression in the gastrointestinal tract by various mechanisms. For example, Fusobacterium nucleatum, which primarily inhabits the oral cavity and causes periodontal disease, might contribute to aggressive tumor behavior through activation of chemokines such as CCL20 in esophageal cancer tissue. Composition of the intestinal microbiota is influenced by diet, lifestyle, antibiotics, and pro‐ and prebiotics. Therefore, by better understanding how the bacterial microbiota contributes to esophageal carcinogenesis, we might develop novel cancer prevention and treatment strategies through targeting the gastrointestinal microflora. This review discusses the current knowledge, available data and information on the relationship of microbiota with esophagitis, Barrett's esophagus, esophageal adenocarcinoma and squamous cell carcinoma.

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Section: Introductionmentioning

confidence: 99%

Review of the gut microbiome and esophageal cancer: Pathogenesis and potential clinical implications

Baba

Iwatsuki

Yoshida

et al. 2017

Annals of Gastroent Surgery

101

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“…Given the role of epigenetic mechanisms in the regulation of immune functions, notably in the control of Th17 cell and Treg differentiation, it is not surprising that inflammatory diseases are linked to a substantial remodeling of the host epigenome in various tissues [Figure 1; (8–10)]. There is growing evidence that the gut microbial community is critical for the maintenance of a healthy host, and clear links between the gut microbiota and the central nervous system, or the cardiovascular and metabolic functions have been established (11–14). Consequently, perturbations of the gut microbiota (or dysbiosis), encompassing reduced microbial diversity and changes in microbiota composition, have been associated with a large number of chronic conditions (15).…”

Section: Introductionmentioning

confidence: 99%

The Microbiota and Epigenetic Regulation of T Helper 17/Regulatory T Cells: In Search of a Balanced Immune System

et al. 2017

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Immune cells not only affect tissue homeostasis at the site of inflammation but also exert systemic effects contributing to multiple chronic conditions. Recent evidence clearly supports an altered T helper 17/regulatory T cell (Th17/Treg) balance leading to the development and progression of inflammatory diseases that not only affect the gastrointestinal tract but also have whole-body manifestations, including insulin resistance. Epigenetic mechanisms are amenable to both environmental and circulating factors and contribute to determining the T cell landscape. The recently identified participation of the gut microbiota in the remodeling of the epigenome of immune cells has triggered a paradigm shift in our understanding of the etiology of various inflammatory diseases and opened new paths toward therapeutic strategies. In this review, we provide an overview of the contribution of the Th17/Treg balance in the development and progression of inflammatory bowel diseases and metabolic diseases. We discuss the involvement of epigenetic mechanisms in the regulation of T cell function in the particular context of dysbiosis. Finally, we examine the potential for nutritional interventions affecting the gut microbiota to reshape the T cell epigenome and address the inflammatory component of various diseases.

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“…In the last decade, the gut microbiota has emerged as a key regulator of liver physiology through the gut–liver axis (4, 9). Liver inflammation has been associated with an alteration of the gut microbiota composition in patients with nonalcoholic steatohepatitis and alcoholic hepatitis (10, 11).…”

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confidence: 99%

The gut microbiota metabolite indole alleviates liver inflammation in mice

et al. 2018

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The gut microbiota regulates key hepatic functions, notably through the production of bacterial metabolites that are transported via the portal circulation. We evaluated the effects of metabolites produced by the gut microbiota from aromatic amino acids (phenylacetate, benzoate, p-cresol, and indole) on liver inflammation induced by bacterial endotoxin. Precision-cut liver slices prepared from control mice, Kupffer cell (KC)-depleted mice, and obese mice (ob/ob) were treated with or without LPS and bacterial metabolites. We observed beneficial effects of indole that dose-dependently reduced the LPS-induced up-regulation of proinflammatory mediators at both mRNA and protein levels in precision-cut liver slices prepared from control or ob/ob mice. KC depletion partly prevented the antiinflammatory effects of indole, notably through a reduction of nucleotide-binding domain and leucine-rich repeat containing (NLR) family pyrin domain-containing 3 (NLRP3) pathway activation. In vivo, the oral administration of indole before an LPS injection reduced the expression of key proteins of the NF-κB pathway and downstream proinflammatory gene up-regulation. Indole also prevented LPS-induced alterations of cholesterol metabolism through a transcriptional regulation associated with increased 4β-hydroxycholesterol hepatic levels. In summary, indole appears as a bacterial metabolite produced from tryptophan that is able to counteract the detrimental effects of LPS in the liver. Indole could be a new target to develop innovative strategies to decrease hepatic inflammation.—Beaumont, M., Neyrinck, A. M., Olivares, M., Rodriguez, J., de Rocca Serra, A., Roumain, M., Bindels, L. B., Cani, P. D., Evenepoel, P., Muccioli, G. G., Demoulin, J.-B., Delzenne, N. M. The gut microbiota metabolite indole alleviates liver inflammation in mice.

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Gut microbiome and liver diseases

Cited by 412 publications

References 96 publications

Review of the gut microbiome and esophageal cancer: Pathogenesis and potential clinical implications

Review of the gut microbiome and esophageal cancer: Pathogenesis and potential clinical implications

The Microbiota and Epigenetic Regulation of T Helper 17/Regulatory T Cells: In Search of a Balanced Immune System

The gut microbiota metabolite indole alleviates liver inflammation in mice

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